Others and we have shown in several studies that the natural tetrahydropyrimidine ectoine protects mammalian
cells and tissues against various stress factors including ischemia/reperfusion injury, UV-irradiation, and inflammation.
Since little is known about the molecular mechanism of this protective effect, which was ascribed exclusively to an extracellular
action of this small water-soluble molecule, we asked whether and how a hydrophobic anchor modulates the inflammation
protective properties of ectoine. We therefore investigated the influence of ectoine and of its semi-synthetic
derivative lauryl-ectoine on inflammation in RAW 264.7 macrophages and primary cultured rat intestinal smooth muscle
(RISM) cells. Both, ectoine and lauryl-ectoine considerably decreased lipopolysaccharide (LPS)-induced interleukin (IL)-
1, IL-6, tumor necrosis factor (TNF)- α, and cyclooxygenase (COX)-2 gene expression in macrophages as well as TNF-α-
induced IL-1, IL-6 and COX-2 expression in RISM cells. This reduction of inflammatory agents was accompanied on the
one hand by a significant decrease of nuclear translocation of nuclear factor (NF)-κB and on the other hand by a reduction
of cellular ceramide content. Interestingly, lauryl- ectoine was much more active exerting its effect at about 10-fold lower
concentrations than its natural counterpart. Note that ectoine was almost completely recovered in the medium whereas
lauryl-ectoine was found to be cell-associated. Together our data indicate that a lipid anchor considerably improves a possible
preventive and/or therapeutic implementation of ectoine in inflammatory processes.
Keywords: Ectoine, ceramide, inflammation, lauryl-ectoine, lipophilicity, tumor necrosis factor alpha (TNF-α).
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